Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Molecular and functional analysis of sunitinib resistance induction in human renal cell carcinoma cells

ABSTRACT: We report that in response to chronic treatment with the small molecule-based targeted drug sunitinib, human Caki-1 cells alter their pheno- and genotype. We detected that the metabolism of sunitinib is still functional, but sunitinib and its N-desethyl metabolite are accumulated in the interios (lysosmes). Gene expression analysis revealed significant differential expression of genes related to mitosis, apoptosis and cell attachment. We detected potential upregulation of autophagy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE172165 | GEO | 2021/04/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Drug repurposing identifies a synergistic high-order drug combination to treat sunitinib-resistant renal cell carcinoma

Project description:We report that in response to combination treatment with a synergistic low-dose four-drug combination, human Caki-1 cells resistant to sunitinib alter their pheno- and genotype. We detected that the metabolism of these cells is altered. Gene expression analysis revealed significant differential expression of genes related to mitosis, apoptosis and cell attachment. We detected regulation changes in enzymes mediating the ceramide and sphingolipid metabolism.

2021-05-21 | GSE174740 | GEO

Integrated miRNA-genomic analysis of sunitinib resistance in clear cell renal cell carcinoma (CCRCC) cell lines

Project description:clariom D and miRNA v4.0 microarray analyses of 786-O, A498 and Caki-1 cells suntinib resistant cell lines and originator cell lines we used intergrated pathway network analysis to identify miRNA-target gene pairs involved in sunitinib resistance.

2021-09-02 | GSE183140 | GEO

Amiloride reduces FN3K expression to restore sunitinib sensitivity in renal cell carcinoma

Project description:The kidney is a vital organ responsible for water and sodium metabolism, while the primary function of amiloride is to promote the excretion of water and sodium. We investigated amiloride enhanced the sunitinib sensitivity in RCC. We found both sunitinib and amiloride displayed cytotoxicity and exerted the synergy effect in RCC cells in vivo and in vitro arrays. Protein expression profiles were screened via MS/TMT, revealing that FN3K was upregulated in sunitinib group, and rescued in amiloride and the combination administration. Exogenous FN3K could promote proliferation, invasion and metastasis and decrease the sensitivity of Caki-1 cells to sunitinib, also, exogenous FN3K up-regulated VEGFR2 expression and activated AKT/mTOR signal pathway. More FN3K and VEGFR2 accumulated in R-Caki-1 cells and rescued by amiloride treatment. Co-IP and IF confirmed the interaction between FN3K and VEGFR2. In conclusion, FN3K depletion mediated VEGFR2 disruption promotes amiloride synergized the anti-RCC activity of sunitinib.

2024-05-07 | PXD052100 |

Impact of sunitinib resistance on clear cell renal cell carcinoma therapeutic sensitivity in vitro

Project description:Sunitinib resistance creates a major clinical challenge for the treatment of advanced clear cell renal cell carcinoma (ccRCC) and functional and metabolic changes linked to sunitinib resistance are not fully understood. We sought to characterize the molecular and metabolic changes induced by the development of sunitinib resistance in ccRCC by developing and characterizing the transcriptome of two human ccRCC cell lines resistant to sunitinib.

2024-04-17 | GSE216494 | GEO

miRNA array of clear cell renal cell carcinoma from patients treated with sunitinib

Project description:A multiple receptor tyrosine kinase inhibitor, sunitinib, is a first-line therapy for clear cell renal cell carcinoma (CCRCC). Unfortunately, it has the major challenges of low initial response rate and resistance after about one year of treatment. Here we evaluated a microRNA (miRNA) and its target responsible for sunitinib resistance. Using miRNA profiling, we identified miR-96-5p upregulation in tumors from sunitinib-resistant CCRCC patients

2021-12-03 | GSE189331 | GEO

Differentially expressed genes analysis between dihydroberberine, sunitinib and dihydroberberine plus sunitinib.

Project description:To gain insights into the mechanisms of dihydroberberine, sunitinib and dihydroberberine plus sunitinib on inhibition to A549 cells, we have employed whole genome microarray expression profiling as a discovery platform to identify different genes between dihydroberberine, sunitinib and dihydroberberine plus sunitinib-treated sample and control.

2015-06-26 | GSE70282 | GEO

Sunitinib treatment exacerbates intratumoral heterogeneity in metastatic renal cancer

Project description:The aim of this study was to investigate the effect of VEGF targeted therapy (sunitinib) on intratumoral heterogeneity (ITH) in metastatic clear cell renal cancer (mRCC).

2015-05-25 | GSE65615 | GEO

Sunitinib treatment exacerbates intratumoral heterogeneity in metastatic renal cancer (CGH)

Project description:The aim of this study was to investigate the effect of VEGF targeted therapy (sunitinib) on intratumoral heterogeneity (ITH) in metastatic clear cell renal cancer (mRCC). To explore ITH in detail, multiple tumor samples were taken from the primary renal tumors of mRCC patients who were sunitinib treated (n=23) or untreated (n=23). ITH of pathological grade, DNA (using array-based comparative genomic hybridisation), RNA (Illumina Beadarray) and protein (reverse phase protein array) were evaluated. Tumor grade heterogeneity was greater in treated compared to untreated tumors (P=0.002). Unsupervised and supervised analysis, for renal cancer driver, hypoxia and stromal gene signatures, was then performed. In untreated patient tumor samples, significant ITH occurred in chromosomal aberrations, RNA and protein expression, with clustering of DNA and RNA correlating for individual patients. In unsupervised analysis sunitinib therapy was not associated with increased ITH in DNA or RNA. However there was an increase in ITH for the driver mutation and hypoxia gene signatures (DNA and RNA) as well as increasing variability of protein expression with treatment (p<0.05). Despite this variability, significant chromosomal and RNA changes to targets of sunitinib, such as VHL, PBRM1 and CAIX, occurred in the treated samples. Together these findings suggest that sunitinib treatment has significant effects on the expression and ITH of key tumor and treatment specific genes. The results do not support the hypothesis that resistant clones are selected and predominate after initiation of targeted therapy; instead it appears that an initial clonal diversification occurs, supporting the hypothesis of polyclonal drug resistance.

2015-05-25 | GSE67818 | GEO

Sunitinib treatment exacerbates intratumoral heterogeneity in metastatic renal cancer (CGH)

2015-05-25 | E-GEOD-67818 | biostudies-arrayexpress

Expression data from renal cancer xenograft tumor treated with sunitinib or vehicle

Project description:We established 3 types of primary xenograft models (KURC;Kyoto University Renal Cancer-1,2,3) derived from human renal cell carcinoma tissues, and 40 mg/day of sunitinib was orally administered. We performed microarray analysis to compare the gene expression profile of sunitinib-treated primary xenograft tumors (sensitive or resistant status) with that of vehicle-treated.

2015-03-10 | GSE66346 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data